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My Lp(a) Levels are High: Here’s What I’m Doing About it

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To understand Lipoprotein (a) or “Lp(a)” for short, it’s necessary to first grasp a few concepts related to LDL, so that is where I will begin.

LDL-C vs. Lp(a)

Everyone has heard of LDL-C, or “bad cholesterol.”

However, LDL-C isn’t really cholesterol at all, instead it’s the measurement of the weight of the cholesterol inside of special carrier proteins called low density lipoproteins (LDL). Lipoproteins, of which LDL are one sub-type, are “fat taxis,” they carry various types of fats throughout the body.

And even though they play a critical role in our metabolism, LDL are not our friends when they become too numerous. The European Atherosclerosis Society recently published a consensus paper calling LDL the key driver of heart disease. 1 If you are in the low carb camp and don’t believe significantly elevated LDL is an issue, this blog post probably isn’t for you.

As a general rule, you want lower LDL-C for optimal cardiovascular health. This is the case because the process of heart disease begins with a lipoprotein delivering an errant piece of cholesterol to the artery wall, where it gets “stuck.” Immune cells come to the site of the injury to try to dislodge the cholesterol particle, and sometimes they are successful. However, as the number of lipoproteins carrying cholesterol increases, it becomes more and more likely that one of these lipoproteins will take a wrong turn and deliver cholesterol (or a phospholipid) beneath the cells that line the blood vessels where it stays in place, thus setting off the inflammatory state that leads to heart disease. 2

As the image below helps elucidate, the shell of LDL particles are comprised of special proteins called apolipoprotein B, or “APOB” for short. For more on APOB, and why it is an important metric for gauging heart health, see this blog post. By contrast, the protein that makes up HDL, sometimes called “good cholesterol” is called apolipoprotein A, or APO(a).

You can think of Lp(a) as a type of “genetic bad cholesterol” with a special hybrid protein structure. Those who carry variants in the LPA family of genes are much more likely to have elevated Lp(a) levels. 3

In structure, Lp(a) is a cholesterol rich APOB containing LDL particle that has an extra APO(a) protein tail added on, hence the “little a.” 4

Image credit: https://www.amgenscience.com/features/10-things-to-know-about-lipoproteina/

Lp(a) testing is rare

Although elevated levels of Lp(a) are a direct risk factor for heart disease and are thought to increase risk significantly, most “normal” lipid panels don’t even measure for Lp(a). 5

In fact, when I get Lp(a) tests done my insurance carrier often sends me a letter saying the test isn’t proven and therefore isn’t covered.

In the standard lipid panel that most of us get, Lp(a) “hides” in the LDL-C number. What I mean here is that, absent a break out for Lp(a) specifically, Lp(a) will be included in your overall LDL-C number. 6 As the latest update in my Lp(a) numbers shows on the table below, I have had blood tests where my Lp(a) has been high despite LDL-C numbers that are close to optimal at just over 100 mg/DL.

When all they get is an LDL-C test, the result for those with a genetic predisposition to high Lp(a) can be statin prescriptions that may not be as efficacious as they would be under the more “normal” circumstance of high LDL-C, but low Lp(a). 7

To quote a study from Kidney International.

Since statins have no influence on Lp(a) levels, it can be expected that the LDL cholesterol-lowering effect of statins may be diminished in patients who have a pronounced elevation of Lp(a) levels accompanied by only moderate elevations of LDL cholesterol.

In this study, when LDL numbers were adjusted for Lp(a), 25.7% of the patients in the study had LDL levels that were no longer in need of statin intervention.

Having said that, if your doctor recommends a statin, it is wise to follow his or her advice.

What constitutes “high” Lp(a)?

The Framingham study reported a 2 to 3 times increased risk for heart disease when Lp(a) levels are greater than 30mg/dl, or 75 nmol/L. 8

However, not all medical bodies see eye to eye on what constitutes dangerous Lp(a) levels. The European Atherosclerosis Society (EAS) lists Lp(a) numbers of >50 mg/dl as elevated and as the starting point for concern. 9

The Fourier trial established that Lp(a) is a risk factor for heart disease independent of where your LDL-C sits (the old thinking had been that if you get LDL-C low enough, Lp(a) becomes a non-factor). 10

We have seen very public examples of how elevated Lp(a) can do damage, even early in life. Celebrity trainer Bob Harper, of Biggest Loser fame, suffered a heart attack at age 52 when he appeared to be in his prime. As it turns out, the culprit was elevated Lp(a).

Bob’s doctors hadn’t tested him and so he never knew he was at increased risk for heart disease.

Even had he known, could Bob have lowered Lp(a) enough to avoid a heart attack?

The subject is a matter of some controversy. Unlike other cardio related biomarkers, Lp(a) numbers are primarily driven by genetics and are therefore tough to move with diet and drugs.

Lp(a) inversely associated with triglyceride levels

So, we have a ballpark of what constitutes high Lp(a), but who is more likely to have higher Lp(a) levels? Interestingly, Lp(a) is inversely associated with high triglyceride levels and with type 2 diabetes. 11

Interestingly, you can see this trend show up in my blood work in the chart below.

My lowest every Lp(a) levels resulted from my worst ever blood draw, one I did after a period of very poor eating, and too much drinking. The bad diet habits I engaged in for a number of days spiked my triglycerides, but put my Lp(a) into the green zone for the first time ever.

This is not to say that the strategy for reducing Lp(a) should be to shoot for high triglycerides, another risk factor for heart disease. However, it’s worth noting as keeping triglycerides on the higher side of optimal, as they often are on vegetarian diets, could be preferable for those looking to manage Lp(a).

How I discovered elevated Lp(a)

Lp(a) first came on my radar after doing a Boston Heart Diagnostics Cardio panel. My lipid markers were generally ok, but at 43 mg/dl on one test, and with previous results at 46 and 49 mg/dl, my Lp(a) number was labeled “borderline.”

After reviewing my charts, my doctor told me there wasn’t much I could do to lower Lp(a).

“Lp(a) is genetic, you can’t change it all that much. It’s possible Niacin could help”

That’s never fun to hear for a metric that is tied to increased risk of heart disease, but I resolved to try nonetheless.

As you can see from the chart below, I was able to drop my Lp(a) number down to 33mg/dl by focusing on lowering my LDL-C and LDL-P numbers.

You’ll also see that my Lp(a) numbers spiked when I ate a diet high in cholesterol.

Differences in Lp(a) reporting

Interestingly, Boston Heart Labs lists Lp(a) results on its Cardio panel in mg/dl, while the Quest Diagnostics Cardio IQ panel lists Lp(a) results in nmol/L.

I had a Boston Heart panel done, and then followed up a week later with a Cardio IQ panel from Quest. I was looking for a disparity between the mg/dl number and the nmol/L number to try to prove, or disprove, the theory that nmol/L is the most accurate way to measure for Lp(a), and that as a weight based measurement, mg/DL doesn’t give you the whole picture.

Unsurprisingly, my labs came back with an Lp(a) of 43 mg/dl and 98 with a nmol/L measurement, in the borderline category on both tests.

How I lowered my Lp(a)

When I first learned that I had elevated Lp(a), I was concerned. I was especially concerned because many say there isn’t much you can do to lower Lp(a).

Having said that, since I first found out about elevated Lp(a) levels, I’ve moved my number down 16 points (33%), from a high of 49 mg/dl to my new low of 33 mg/dl. Again, this is not scientific, but between blood draws, which I do every 3-4 months, I experiment with different nutritional strategies.

I have confirmed, both by genetic testing as well as through extensive blood work, that I tend to hyper absorb cholesterol. This is why I went on Zetia for a stretch.

As a result, it’s probably not a surprise that I achieved one of my lowest Lp(a) numbers (43 mg/DL) after shifting to a largely plant based diet, completely getting rid of added butter (when I go out to eat all bets are off if butter is included in a dish), eating egg whites instead of the whole egg, and eating red meat very sparingly, if at all.

I achieved my 33mg/dl number after transitioning to a 85-90% plant based diet. So, essentially, I ignored most of the Bulletproof ketogenic diet themes and lowered the amount of animal protein and animal fat I was consuming. I ate Vegan a few days a week and almost always had a plant based breakfast and lunch. In short, I ate a lot less meat and a lot less saturated fat. I would still eat eggs once or twice a week, wild salmon, and some lean chicken, but I became a vegetarian for the most part.

I am not suggesting this will work for everyone, it’s just what seemed to work for me.

Notice in my data below that my best Lp(a) number (where I moved it to the green at a 72 nmol/L level) was on the same draw where I experimented with deliberately eating a junk food diet (pizza and mezcal) to see what my blood would look like. My particle count got scary high, but Lp(a) went to the lowest level ever. The 72 nmol/L is about 29 mg/dl by my estimation. The only thing I could speculate about as to why the number was so low was high dose Vitamin C (1,000 mg a day), as well as the documented inverse relationship between Lp(a) and triglyceride levels, but this is obviously less than scientific.

You’ll also see what happened to my Lp(a) numbers after eating about 17 eggs a week for about two months. My LDL-C, total cholesterol, and even APOB were all in range, but my Lp(a) and LDL-P went a little higher than I would like to see.

John's Lp(a) progress

 
LDL-P
LDL - C
Lp(a)
Total cholesterol
Triglycerides
August 2016
1100
113
49
174
94
February 2017
1147
107
43
171
101
November 2017
931
93
33
157
66
September 2018
85 APOB
110
40
182
91
November 2018
79 APOB
119
DNT
191
87
April 2019
1732
120
72 nmol/L
215
277
June 2019
1302
92
80 nmol/L
167
112
March 2020
87 APOB
108
113 nmol/L
183
115

Reducing Lp(a) risk by attacking LDL-P – still a sound strategy in light of Fourier?

According to lipid expert Tom Dayspring’s older work, which reflected the previous thinking on Lp(a), Lp(a) wasn’t thought to be a risk factor when LDL-C was normalized.

To quote a section of Tom’s old Lp(a) paper, which actually quotes another doctor named Dr. Greg Brown:

In an analysis by Maher et al. of the Lp(a) data in the FATS trial, lowering LDL levels in those with high LDL and high Lp(a) levels dramatically reduced risk. Without treatment, these patients had a 42% risk of a major clinical event, including MI, the need for revascularization, or CV death over the 2.5 year study. When LDL levels were lowered aggressively, even though the Lp(a) levels remained high, the risk of this group was reduced to less than 10%, for a roughly 75% reduction in the risk of a major cardiovascular event. While Lp(a) (and probably risk) may be modestly lowered with niacin therapy, and with estrogens in women, aggressive lowering of LDL levels appears to be the most reliable way to treat patients at high risk due to elevated Lp(a).

This has changed in light of Fourier – meaning high Lp(a) is a risk factor for heart disease independent of LDL-C.

That’s the bad news.

BUT, the good news seems to be that the practical approach for someone with elevated Lp(a), is to aggressively target LDL-P and cholesterol rich LDL particles in particular. I say this because that is what PCSK9 inhibitors do, they accelerate the clearance of cholesterol out of circulation and into the liver.

So, if you’re Lp(a) is off the charts high, the consensus view seems to be that you must target the LDL-P number more aggressively.

The Maher study linked to above is from 1995. I hope to have Tom on the podcast in the next few months to get his current thinking on to what extent low LDL-C reduces the risk from elevated Lp(a).

The Cleveland Clinic references a study on this blog page, without citing or linking to it, that looked at 5,000 patients with elevated Lp(a). When the LDL in these patients was brought down (not specified whether this was LDL-C or LDL-P), the “increased risk for mortality from Lp(a) was negligible.”

These are the studies that offer good news for those of us who need to keep an eye on Lp(a). Since Lp(a) is carried on the LDL particle, it needs LDL to do damage.

The less LDL to bind to, the less Lp(a).

Reasons for elevated LDL-P

In cases where triglycerides are high, insulin resistance (and therefore triglyceride rich particle) can be the primary driver of LDL-P.

Another scenario that can rear its head is heightened cholesterol synthesis, absorption, and poor clearance. This means that some of us will make more cholesterol in response to a higher fat diet. The result is more cholesterol rich LDL-P and more risk added on top of Lp(a).

The idea here is that, in insulin resistant patients, the LDL particle is packing greater amounts of triglycerides (produced from sugar) than cholesterol. This puts the LDL-C number low, but the LDL-P, the true predictor of bad heart outcomes, high.

Taking care of the insulin resistance with metformin or dietary interventions, reduces the LDL-P count, i.e. the number of LDL-P that are moving triglycerides around. This is a perfectly logical result in those with high triglycerides (as was the case with the case study) and high LDL-P, but not as much in cases where LDL-P is elevated and triglycerides are low.

In those cases, where the LDL particles are cholesterol rich and metabolic syndrome can be effectively ruled out, we can’t rely on a “cholesterol depleted” lipoprotein theory.

In cases where the LDL-C number is high, and triglycerides are low, the method of attack is more likely to be a diet that is very low in fat and cholesterol.

For more on lowering LDL-C, check out this post: Why is my LDL-C high and what can I do to lower it?

Lysine and vitamin C

Also known as the Linus Pauling Lp(a) protocol, this regimen calls for 3g of Vitamin C and 3g of Lysine a day.

There is some chatter indicating that Lysine and vitamin C supplementation can reduce Lp(a) numbers because lysine binds to Lp(a) particles. The lysine doses recommended sound very high to me, and I would imagine they would come with side effects for many people.

Does Niacin lower Lp(a)?

When I first saw a blood panel that had elevated Lp(a), my doctor began discussing Niacin as a supplement, as there is some data to suggest that Niacin can effectively reduce Lp(a) levels, although this study suggests that Niacin’s effectiveness may vary based on Apo(a) phenotype and it is my understanding that Niacin has generally fallen out of favor with most top lipidologists.

Consider this quote from lipid expert Tom Dayspring, M.D. from his paper titled Lp(a):

The drugs that inhibit hepatic apo (a) synthesis (niacin, fenofibrate, estrogen, raloxifene) will cause less apoprotein (a) to be attached to LDL particles. These drugs reduce Lp(a) levels but none as monotherapy are particularly efficacious as statins in reducing LDL-P or LDL-C. There are no outcome studies relating clinical event reduction to what a drug does to Lp(a) levels. There are all sorts of studies showing lowering LDL-C or LDL-P saves lives and that is why those surrogates are what NCEP strongly suggests clinician’s direct therapy at. Some advocate the use niacin to lower apo (a) levels, yet there is no clinical trial evidence whatsoever that clinical events would be affected. Many people have extremely high Lp(a) levels. Niacin can only lower it 25-30% which would never get the Lp(a) concentration close to a normal level.

What I hear Tom saying is that trials aimed at lowering Lp(a) are almost by definition performed in people with very elevated Lp(a). None of the trials in these people can normalize Lp(a) using niacin, and as a result, cardiovascular risk remains high.

It remains high UNLESS you lower LDL-P and LDL-C. Remember that the APO(a) tail has to bind to an LDL particle to be dangerous. The fewer LDL particles, the fewer opportunities for APO(a) to do damage.

So, as a practical matter, just bringing down Lp(a) is not the right call unless you are getting really serious about LDL-P.

If the Lp(a) number is only borderline high, perhaps there is a benefit in lowering Lp(a), especially if you can get levels to a normal range. Against this backdrop, it may not matter if you lower Lp(a) unless you are also lowering the overall particle count.

The bottom line here is twofold:

  1. Niacin supplementation has been shown to lower Lp(a) levels significantly.7
  2. Niacin has side effects such as flushing and insomnia.8

Omega 3 fish oil and Lp(a)

This one surprised me. As you can see from the table above, there are a series of studies that show omega 3 fish oil, sometimes alone and sometimes combined with other supplements and diet changes, lowers Lp(a).

If you’re in the market for fish oil products, check out our guide to Omega 3 fish oil, which I only half jokingly titled “Most Fish Oil is Garbage. Here’s What to do About it.”

Additional resources and key takeaways

For me, the key takeaway here is that elevated Lp(a) is a sign that an individual must be even more vigilant about maintaining proper “cardiovascular hygiene.” Although Lp(a) may not move with ease, it’s worth the effort to determine what drives your LDL-P number and make the changes you need to to get that number in line, which usually will mean less than 1,000.

For an epic explanation of how our body’s use cholesterol, and which metrics actually matter for heart disease, I highly recommend Dr. Peter Attia’s lengthy, but excellent, series: the Straight Dope on Cholesterol.

Aaron also put together a valuable summation of the interplay between cholesterol, heart health, and genetics on this Gene Food blog, which is worth a read.

John O'Connor

John O'Connor is the founder of Gene Food, host of the Gene Food Podcast and a health coach trained at Duke's Integrative Medicine Program. Read his full bio here.

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